Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

752
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
752
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

416
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
416

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

High-Temperature Persistent Luminescence and Anti-Thermal Quenching in LiGa<sub>5</sub>O<sub>8</sub> by Trap Engineering.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Kaempferol Attenuates Spaceflight-Associated Knee Cartilage Degradation by Targeting NOX4-Mediated Mitochondrial Dysfunction.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Distinct orbitofrontal circuits with dorsal and ventral CA1 differentially regulate spatial memory and emotional behaviors.

Frontiers in behavioral neuroscience·2026
Same author

Holistic genome assembly and analysis of the <i>Tremella fuciformis</i> interaction community uncovers intergenomic insights beyond dual genomes.

IMA fungus·2026
Same author

Effects of post-activation performance enhancement added to general warm-up on jump, sprint, and change-of-direction performance in competitive athletes: a systematic review and meta-analysis.

BMC sports science, medicine & rehabilitation·2026
Same author

Li<sup>+</sup>-Mediated Topological Regulation of Aluminosilicate Glass Ceramics: Near-Full Crystallinity for Multifunctional Optoelectronic Applications.

Advanced materials (Deerfield Beach, Fla.)·2026

Related Experiment Video

Updated: Jan 18, 2026

Light-sheet Fluorescence Microscopy to Capture 4-Dimensional Images of the Effects of Modulating Shear Stress on the Developing Zebrafish Heart
06:51

Light-sheet Fluorescence Microscopy to Capture 4-Dimensional Images of the Effects of Modulating Shear Stress on the Developing Zebrafish Heart

Published on: August 10, 2018

8.8K

VEGFC/VEGFR3 Signaling-Dependent Lymphatic Remodeling Modulates Cardiac Response to Pressure Overload.

Lina Su1, Yuxia Cui1, Manyan Wu1

  • 1Department of Cardiology, Beijing Key Laboratory of Early Prediction and Intervention of Acute Myocardial Infarction, Center for Cardiovascular Translational Research Peking University People's Hospital Beijing China.

Journal of the American Heart Association
|September 11, 2025
PubMed
Summary

Targeting cardiac lymphangiogenesis with vascular endothelial growth factor C (VEGFC) shows promise for heart failure treatment. Enhancing VEGFC/VEGFR3 signaling promotes lymphatic remodeling and reduces inflammation, offering a potential noninvasive therapy.

Keywords:
VEGFC/VEGFR3 signalingYAPheart failurelymphatic vesselspressure overload

More Related Videos

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

5.5K
A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
07:13

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

Published on: April 30, 2020

6.9K

Related Experiment Videos

Last Updated: Jan 18, 2026

Light-sheet Fluorescence Microscopy to Capture 4-Dimensional Images of the Effects of Modulating Shear Stress on the Developing Zebrafish Heart
06:51

Light-sheet Fluorescence Microscopy to Capture 4-Dimensional Images of the Effects of Modulating Shear Stress on the Developing Zebrafish Heart

Published on: August 10, 2018

8.8K
Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

5.5K
A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
07:13

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

Published on: April 30, 2020

6.9K

Area of Science:

  • Cardiovascular Biology
  • Lymphatic System Research
  • Molecular Medicine

Background:

  • Cardiac lymphangiogenesis is a potential therapeutic target for heart failure.
  • Systemic vascular endothelial growth factor C (VEGFC) delivery shows inconsistent results in promoting cardiac lymphangiogenesis.
  • Mechanisms of lymphatic remodeling in heart failure are not well understood.

Purpose of the Study:

  • To investigate the role of lymphatic remodeling in heart failure.
  • To determine the efficacy of modulating VEGFC/VEGFR3 signaling in heart failure.
  • To elucidate the role of Yes-associated protein in VEGFC/VEGFR3 signaling.

Main Methods:

  • Adeno-associated virus (AAV)-mediated gene therapy in mice subjected to transverse aortic constriction (TAC).
  • AAV-sh-VEGFR3 to inhibit vascular endothelial growth factor receptor 3 (VEGFR3) expression.
  • AAV-VEGFC to enhance VEGFC expression.
  • In vitro studies on lymphatic endothelial cells.

Main Results:

  • TAC induced adaptive cardiac lymphangiogenesis and enhanced peripheral lymphatic transport.
  • Inhibition of VEGFR3 exacerbated cardiac inflammation and adverse remodeling.
  • VEGFC therapy was cardioprotective, promoting lymphangiogenesis and resolving inflammation.
  • VEGFC treatment improved lymphatic drainage and reduced peripheral congestion.
  • Yes-associated protein dephosphorylation is crucial for VEGFC/VEGFR3 signaling.

Conclusions:

  • Targeting cardiac lymphangiogenesis via VEGFC/VEGFR3 signaling is a promising therapeutic strategy for heart failure.
  • VEGFC administration may serve as a noninvasive decongestive approach in heart failure management.
  • Modulating the lymphatic system offers a novel therapeutic avenue for heart failure.